Volume 12

Treasury of human inheritance / edited by Karl Pearson, R.A. Fisher, L.S. Penrose.

Date:
1909-
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: Treasury of human inheritance / edited by Karl Pearson, R.A. Fisher, L.S. Penrose. Source: Wellcome Collection.

    33/102 (page 95)
    than has been demonstrable in some other diseases of the same genetic type; possible examples of this can be seen in Figs. 171, 190, 201, 202, 204, 205, 207 and 212; in some of these cases no doubt the parent who transmitted died before any real freedom from manifestation was determined. Table 10 Parents of Group C No. of sibships Affected Unaffected Percentage of sibship affected* <? ? <? ¥ Mother affected 79 92 83 70 55 52-5 Father affected 75 86 96 74 30 52-1 One parent affected 154 178 179 144 125 52-3 Both parents normalf 23 39 28 33 19 51-9 * Includes members whose sex is not given. t Not directly comparable with other entries as this group includes only sibships in which affected individuals have occurred. My material includes 79 sibships, of whom the mother was affected, and 75 sibships, of whom the father was affected; it will be seen from the table above that in both cases the proportion of affected amongst the offspring is similar and closely fulfils the expectation of 50 % for the genetic type concerned. An extremely interesting point that has emerged from this work is the possibility of linkage of peroneal atrophy with inability to taste phenyl thiocarbamide in the family of Fig. 167; at Professor Fisher’s suggestion I tested as many of the family as were available and who consented to collaborate; of these, it will be observed from an examination of the pedigree (a) That amongst the descendants of II. 1, the five individuals with peroneal atrophy were non-tasters, whereas all the tested individuals who remained free from the disease tasted the bitter substance; this fact alone proves nothing because we were unable to test II. 1 and her husband who were no longer living. ( b ) All the descendants of II. 3 appear to be tasters and have married tasters so that we can learn nothing from them, (c) III. 33, a taster with peroneal atrophy, married a non-taster; of their three children those with peroneal atrophy are non-tasters, the son who is free from the disease tasted the bitter substance. It is a misfortune that the affected sister of III. 33, with three still unaffected daughters, refused to collaborate by making the test. The main interest in this experiment lies in the fact that it illustrates the sort of aid to prediction concernmg the liability to manifest inherent hereditary defect which such tests—when information is more complete—may supply. The scope of investigations of this kind is sure to widen and provides, at the present time, the most hopeful outlook concerning the possibility of determining the presence of inherent defect before it becomes manifest in the individual and potential in his offspring; anybody who has talked to the, as yet unaffected, members of stocks carrying, say Huntington’s chorea, must realise the enormous benefit it would be to these people if they could be assured early in life that they need have no fear of the disease developing in themselves or in their children if they marry. 4-2